The Effect of Glucocorticosteroids on Eosinophil Apoptosis Primed by Cultured Nasal Polyp Epithelial Cell Supernatant.
- Author:
Seung Heon SHIN
1
;
Mi Kyung YE
;
Jae Wook CHOI
;
Sang Kyung KIM
;
Hyo Soon JEONG
;
June Sik PARK
Author Information
1. Department of Otolaryngology, College of Medicine, Catholic University of Taegu, Taegu, Korea. hsseung@cuth.cataegu.ac.kr
- Publication Type:Original Article
- Keywords:
Eosinophils;
Glucocorticoids;
Nasal polyps;
Apoptosis
- MeSH:
Apoptosis*;
Asthma;
Budesonide;
Caspase 3;
Culture Media, Conditioned;
Dexamethasone;
Diethylpropion;
Eosinophilia;
Eosinophils*;
Epithelial Cells*;
Glucocorticoids;
Humans;
Nasal Polyps*;
Rhinitis;
Triamcinolone;
Fluticasone
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2000;43(11):1196-1201
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Eosinophil infiltration into inflammatory site is a characteristic histological finding in patients with allergic rhinitis, bronchial asthma, and nasal polyps. The regulation of eosinophil survival and apoptosis may play a major role in tissue eosinophilia, and glucocorticosteroids (GCs) have been used therapeutically for nasal polyps. The purpose of this study is to investigate the effect of commonly used GCs on eosinophil survival and apoptosis primed by nasal polyp epithelial cells. MATERIALS AND METHODS: Peripheral blood eosinophils were incubated in increasing concentrations (10-10M) to GCs (triamcinolone, dexamethasone, budesonide, and fluticasone propionate) from January, 1990 to December, 1999 prior to the addition of human nasal polyp epithelial cell conditioned media (HECM). Eosinophil viability was measured with a MTS assay and apoptosis was analyzed with the caspase-3 staining. RESULTS: GCs suppressed the HECM induced prolongation of eosinophil survival with apoptotic change of cells from 2 days after incubation. Fluticasone propionate showed the strongest effects and triamcinolone showed the weakest effects. CONCLUSION: GCs may diminish eosinophilic infiltration into nasal polyp by decreasing eosinophil viability, and abrogate the promoting effect of nasal epithelial cells.
